Incomplete LBBB, posterior STEMI, posterior leads, in a snowstorm

A 76 yo male had Chest Pain followed by a cardiac arrest. He was resuscitated in the field, and had hypotension annd electrical storm in the ED.


There is a QRS duration of 120 ms, with a wide R-wave in lateral leads (but also a Q-wave). This is either an incomplete LBBB or a very wide left anterior fascicular block. There is concordant ST depression in precordial leads.
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Posterior leads were applied (V4=V7, V5=V8, V6=V9) for the following ECG:

There is now clearly concordant ST elevation. Whether LBBB or not, ST elevation of 0.5 mm or more in just one lead is enough for the diagnosis of posterior STEMI.

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Electrical storm continued, with 8 defibrillations.

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Unfortunately, there was a storm outside, too. A huge snowstorm, and the cath lab personnel could not get to the ED fast enough.

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Tissue plasminogen activator was given and 30 minutes later the patient stabilized with a BP of 130/70. Echo showed a posterolateral wall motion abnormality. Later cath showed 3-vessel disease but the exact culprit could not be established. The troponin I peaked at 40 ng/ml.

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Unfortunately, in spite of therapeutic hypothermia, the patient died of cerebral anoxia.

LAD occlusion in the setting of paced rhythm

An 80 yo male presented with chest pain.


There is clearly a ventricular paced rhythm. Normally in a paced rhythm, the QRS is all negative from V1-V6 because the pacing wire is in the apex of the RV and thus all depolarization goes away from the apex.
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In the above ECG, the QRS in V2 is positive and all others are negative, as in the patient's previous ECG below. This implies some problem with lead placement. Nevertheless, leads V1, V3, and V4 have excessively discordant ST segments.
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Though there is not a lot of data to support it, the ratio used for left bundle branch block seem to be applicable to paced rhythm. An ST/S ratio in V1-V4 > 0.20 is, I believe, quite specific for LAD occlusion. V2, though suspect because of the positive QRS, has a concordant ST segment, which is diagnostic of STEMI.

Previous ECG 2 months prior:


The emergency physician needed to do some persuasion with the interventionalist, but succeeded and the patient was taken for angiography and PCI of a 100% LAD occlusion.

This is the ECG 2 days later:



This is a much more difficult ECG because only complexes 4 and 5 are paced now. The precordial leads have an RBBB morpholoyg, with some minimal persistent ST elevation in v2 and V3 with T-wave inversion, suggestive of reperfusion.

Ischemic symptoms and a paced ECG with excessive discordance in V1-V4, with ST/S ratio > 0.20, is anterior STEMI until proven otherwise.

Weakness due to Bradycardia 2nd Degree Sinoatrial block, with Ashmann's phenomenon

A 68 yo female with a history of HTN on metoprolol and of paroxysmal atrial fib presented with weakness. This is her ECG.

There is sinus bradycardia at a rate of about 55, with a p-wave every 1.05 seconds. There are 2 dropped p-waves. The succeeding p-wave in each case is exactly 2.1 seconds later. This means that the sinus node continues to depolarize and do its pacemaking job every 1.05 seconds, but that occasionally that signal fails to leave the sinus node and get to the atrium where it would depolarize the atrium resulting in a p-wave.

Notice that the p-wave that comes directly after the 8th QRS conducts, but the one that comes after the 4th QRS does not.  This is Ashmann's phenomenon: the refractory period of a beat is longer when the preceding R-R interval is longer.  In this tracing, it is not obvious (you must measure it), but the R-R inverval between R-waves 3 and 4 is longer than the R-R between R-waves 7 and 8.

She was also found to be hypothyroid.

This is sino-atrial exit block. The sinus node fires but it does not escape. The combination of bradycardia (exacerbated by metoprolol), with paroxysmal atrial fib and sino-atrial block are typical of sick sinus syndrome. It will inevitably progress to the point where a pacemaker will be necessary.

Cardiac Arrest, hypotension, tachycardia

A 65 yo woman had felt ill for 36 hours, had seen her MD but without undergoing a cardiac evaluation. She collapsed and 911 was called; she was found pulseless. After epinephrine, atropine, and defibrillation x 2, there was a return of pulses. Exact rhythm during arrest is uncertain. The patient presented with a bp of 90/60 and heart rate of 140. Here is the initial ECG:
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There is sinus tach with PACs. The axis is vertical and down, and is suggestive of left posterior fascicular block (small r in aVL followed by deep S-wave). There is ST depression in II, III, and aVF that is concerning for reciprocal depression from high lateral STEMI in aVL, where there is some ST elevation. There is also ST depression in precordial leads, greatest in V3 and V4, concerning for posterior STEMI. However, with widespread ST depression, this could also be due to diffuse subendocardial ischemia.
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Arguing for posterior STEMI are two things: 1) precordial ST depression is not pronounced in V5 and V6; 2) T waves are inverted away from the ST segment deviation in aVL (down) and in II, III, aVF (up) and in V3 and V4. This is all highly suggestive of posterolateral STEMI that is either subacute or reperfused, but not very acute (in the acute phase, T-waves are upright with the ST elevation).
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Everything is complicated by the arrest and hypotension: Is the ischemia caused by the instability, or the instability caused by the ischemia? What was the inciting factor?
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The diagnosis is in doubt.
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Thus, a bedside echo was performed by the emergency physician and is shown 30 seconds into this video:

65 yo F witnessed arrest from hqmeded.com on Vimeo.
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For those who haven't watched the video, it shows pericardial clot, consistent with myocardial rupture. The patient was taken to the OR by cardiovascular surgery and found to have a necrotic lateral wall with a ventricular leak. The patient died is spite of resuscitative efforts.
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Myocardial rupture is not uncommon. It is found on 1% to 3.5% of autopsies of patients who died of MI. It is associated with transmural MI; since most STEMI are aborted with reperfusion therapy, it is not as common as it once was. It is more common in women, and in patients who have a first MI and have a good EF, as it requires a pump force from the healthy myocardium to produce high pressure which ruptures the infarcted myocardium. The "rupture" is not an explosion, rather a small tract through the myocardium which leaks blood into the pericardium, and kills by tamponade.
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Myocardial rupture is usually preceded by postinfarction regional pericarditis (PIRP). PIRP is indicated on the ECG by 2 findings: 1) persistenly positive (upright) T-waves at 48 hours, or 2) premature reversal of inverted T-waves to positive deflection by 48 to 72 hours after STEMI. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual. There should be QS-waves indicative of completed transmural MI.
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Patients who present with chest pain or cardiac arrest and have an ECG diagnostic of STEMI could have myocardial rupture. Obviously, administration of heparin and/or lytics is hazardous. These patients may survive. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. 5 of 6 presented with chest pain and an ECG indicating reperfusion therapy, but were detected by bedside ultrasound.
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Plummer D et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of EM 23(6):1333-1342; June 1994.
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For more information, see chapter 28 of Smith's "The ECG in Acute MI."

Two more Cases of Takotsubo Stress Cardiomyopathy

Case 1.

This is the ECG of a 50 yo old woman who collapsed, was found to have a pulse, but then found to be in ventricular tachycardia. She was shocked into sinus rhythm. She presented to the ED comatose.

There is marked ST elevation especially in leads V3 to V6, as will as limb leads I and II, with no reciprocal ST depression. The cath lab was activated for STEMI, but the patient had clean coronaries. Before initiating therapeutic hypothermia, a head CT was done and showed fatal subarachnoid hemorrhage.

Case 2.

This 81 yo was found comatose.
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There is ST elevation in V1-V3 with hyperacute T-waves and Q-waves in V2 and V3. This is highly suspicious for acute anterior STEMI. However, she was found to have a fatal pontine hemorrhage and had a maximum troponin I, at 12 hours after presentation, of 2.0 ng/ml. Echocardiogram showed an anteroapical wall motion abnormality. In this case, since no angiogram was done, it is not proven that she did not have a simultaneous anterior STEMI, but with a low maximum troponin and alternative explanation, it is highly unlikely.
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These cases demonstrate that SCM can present with STEMI pseudoinfarction patterns.

Takotsubo Stress Cardiomyopathy

Unfortunately, the ultrasound images of this case were lost.

Briefly, this woman without significant cardiac history went into pulmonary edema with respiratory failure. Her ED echo (not shown) is diagnostic of apical ballooning, also known as "stress cardiomyopathy" (SCM) or "takostubo cardiomyopathy" (because the heart, with its apical ballooning, resembles the Japanese octopus trap called a "takostubo"). The contraction at the base of the heart remains intact, while contraction of the distal or apex is very poor.

Here is the first ECG after the patient became ill.

There is sinus tach with some anterior ST elevation, however not an alarming amount.

Several hours later, she had this ECG recorded:

There is anterior T-wave inversion and very long QTc (680 ms). These are classic SCM findings after the hyperacute phase.


This ECG was recorded the following day:

The QTc is even longer now, at > 700 ms. T-waves are bizarre.

The coronaries were clean, the troponin had a small bump, and the patient recovered. The apparent trigger was stress from losing custody of children.

SCM may happen from a wide variety of psychological or physiological stresses, including respiratory failure (although in this case a psychological stress led to poor myocardial function and then pulmonary edema, then respiratory failure) and intracranial bleeding.

In this case, the ECG never mimicked a STEMI. I will proceed to post a couple cases in which SCM does mimic STEMI.

Computer misses again -- two cases: one very obvious, one very subtle

Case 1.

A 63 year old male had chest pain and syncope after playing hockey (this is Minnesota). A prehospital ECG showed inferior ST elevation and the cath lab was activated by paramedics from the field. Initial BP was 96/60 with a pulse of 65. While waiting for the cath team, an ED ECG was recorded.



This is an obvious inferior STEMI. However, the computer algorithm read "ST elevation with normally inflected T-waves, probably early repolarization. Marked ST depression, probable subendocardial ischemia."

Just remember: if it can be so wrong in this case, then it can also be wrong in the cases you may miss.

There was no right sided ECG available, but a bedside ED echo showed good LV fct, a very large and poorly functioning RV, and a full IVC, all indicative of an RV MI. Volume loading improved blood pressure.

Immediate cath confirmed a very proximal RCA occlusion.


Case 2.

A 67 yo male with h/o mechanical aortic valve and h/o MI stopped taking his coumadin months ago due to depression. In the last couple weeks he has had some CP with exertion. On the day of presentation he had the onset of CP 5 hours previous.

3:01 PM. Read by computer as "nonspecific ST and T wave abnormality"



There is ST elevation of 1 mm in at least 2 inferior leads, and reciprocal ST depression and T-wave inversion in aVL. There is also some ST depression in V2 and V3; any ST depression in these leads is abnormal. This is diagnostic of inferior posterior STEMI.

There was some disagreement about intervention, partly because of the possibility of an emoblism from the valve, and after aspirin and heparin, the patient had some resolution of symptoms, so he underwent a second ECG 1.5 hours later.


4:30 PM

There is now resolution of ST elevation.

The next day, cath revealed an embolism in OM-1, 100% occluded. Peak troponin I was 22 ng/ml. The ECG showed increased T-wave amplitude in V2 and V3, which I have noticed frequently in reperfused posterior STEMI and call "posterior reperfusion T-waves."

ST depression V2-V4: Posterior leads, resolution of pain, and absence of posterior wall motion abnormality ruled out posterior STEMI

I saw this 59 year old male 3 weeks ago. He had no previous history of CAD, and presented with very typical waxing and waning chest pain, much worse with exertion but also present at rest and on presentation, though his pain was minimal at the time of the ECG. Blood pressure was 150/80.

There is sinus rhythm with a normal QRS, except for some increase in R-wave amplitude in V2 and V3, with ST depression in V2-V4. This is all suggestive of posterior STEMI, but not definitely diagnostic.
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A posterior ECG was done and showed no ST elevation, not even 0.5 mm (0.5 mm in only one posterior lead is highly sensitive and specific for posterior STEMI). Aspirin, nitroglycerine sublingual were given and the next ECG showed no change.
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I performed a bedside cardiac ultrasound and the posterior wall appeared to be contracting and shortening normally. IV nitroglycerine was started and titrated up to 60 mcg/min until the pain resolved and a repeat ECG showed near complete resolution of ST depression.
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Heparin and eptifibatide were started for probable NSTEMI, though spontaneous reperfusion (of either the infarct-related artery, or through collateral circulation) of posterior STEMI was not entirely ruled out.
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The ECG normalized overnight. Maximum troponin was 2.1 ng/ml. The patient was taken for angiography which showed severe proximal and mid LAD disease as the culprit. Two stents were placed. The RCA was also severely diseased. There was a new anterior, septal, and apical wall motion abnormality.
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ST depression in V1-V4, isolated, may be either posterior STEMI or NSTEMI. When there is ST depression in precordial leads associated with LAD NSTEMI, it usually stretches out to V5 and V6 (it usually is not maximal in right precordial leads).
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Absence of posterior ST elevation was critical in my decisions on this, as were resolution of symptoms and of ST depression with maximal medical therapy, along with ultrasound showing absence of posterior wall motion abnormality.

If your comment requires a personal response, email me at: dr.smiths.ecg.blog@gmail.com

Cardiogenic Shock and Pulmonary Edema due to Subacute Anterior STEMI

This is a 72 yo male whose symptoms began with a cough 12 hours prior to presentation, at which time he had CP, SOB, and resp distress. On evaluation, he had pulmonary edema and progressive hypotension. His first ECG at 0714 is shown here:

There are QS-waves in V1 and V2, and ST elevation in V1-V3. This morphology is suggestive of either old anterior MI with persistent ST elevation or subacute anterior STEMI. There was a previous ECG on file from one year previous:

This ECG is comparatively normal, without QS-waves or ST elevation. So, at some time between one year ago and the time of presentation, the patient suffered a large anterior MI. That he felt fine until 12 hours ago strongly suggests that the MI began at that time.

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The patient was aggressively supported with mechanical ventilation and pressors. A bedside echo confirmed antero-apical wall motion abnormality. His first troponin returned at 10 ng/ml, confirming subacute anterior STEMI. He went to the cath lab and was found to have a "chronic total LAD occlusion" that received flow from collaterals from the RCA. There was severe 3-vessel disease and also left main disease. A balloon pump was placed and he went for CABG. Here is his post cath ECG.

The ST elevation is resolved. He remains very tachycardic. He is still intubated now. The troponin peaked at 177 ng/ml.

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There was clearly a very significant coronary event. Formal echo confirmed new anterior wall motion abnormality. ST elevation resolved after flow was restored. This was a very large anterior transmural STEMI. One must wonder whether the occlusion was definitely chronic. Clearly, the interventionalist could not cross it with the wire. The exact culprit lesion was not found.

On Vacation, will answer posts when I return (sorry).

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

Here are more examples of wide complex tachycardia: 
these are all a mix of ventricular tachycardia and SVT with aberrancy.

This 51 yo male complained of chest pain, then had a v fib arrest. He was resuscitated and brought to the ED where this ECG was recorded. He was in cardiogenic shock.

There is tachycardia, and there is a wide complex. This wide complex tachycardia could easily be misdiagnosed as V tach. However, there are p-waves, and this is a classic RBBB + LAFB (left anterior fascicular block) morphology. When V tach originates in the left ventricle, there may be an RBBB-like complex, but because VT originates in the myocardium, not in the left bundle (as does RBBB), it does not look exactly like RBBB, as this one does. The left anterior fascicular block can be diagnosed by the left axis deviation. RBBB alone would have S-waves in I and aVL; since there are late large R-waves, there is LAFB.

So now we can say it is sinus tach with RBBB + LAFB.
Is there ST elevation? One must find the end of the QRS in order to determine this. I have done this and marked it up in the image below. The end of the QRS is easy to find in V1. One can then draw a line down to the rhythm strip at the bottom, which is lead II. Thus, you can find where in lead II is the end of the QRS. Then you can go to all parts of the ECG to find the end of the QRS.

As you will see, this results in the discovery of ST elevation in V2-V4 and I and aVL, diagnostic of anterolateral STEMI.

The ED providers activated the cath lab, but the interventionalist refused to come in because it was "not a STEMI".  The patient died 8 hours later of cardiogenic shock.

Early Repolarization vs LAD Occlusion

First ECG in Video

2nd ECG in Video

Critical Hyperkalemia Cases

Pure Posterior STEMI, not a rare event

This 65 yo male presented with 24 hours of intermittent and low grade chest pressure. Here is the presenting ECG:

There is ST depression with upright T-wave in leads V2-V6, maximal in V3. There is no ST elevation anywhere on the ECG. There are those who deny the existence of posterior STEMI; they argue that coronary anatomy makes it "extremely unlikely." But fact has a way of overturning theory.



After therapy with IV nitroglycerine and an aspirin, the ST depression and chest pain resolved. Because of issues with some contraindications to antiplatelet and anticoagulation therapy, and because the ECG and symptoms had resolved, he was not taken immediately for cath. He did have an echo confirming a new posterolateral wall motion abnormality.

Next day cath showed a 100% Ramus intermedius occlusion; it was opened and stented. Max TnI was 14 ng/ml. Echo showed corresponding new WMA and EF was 54%.

There are many studies that indirectly reveal that the percent of STEMIs that are isolated posterior is between 3 and 11% (about 8%). More recently, a substudy of the recent TRITON-TIMI 38 trial comparing Prasugrel to Clopidogrel for ACS enrolled 13,608 patients; 1198 had isolated ST depression in V1-V6. Of these, 314 (26%) had occlusion (TIMI 0 or 1 flow) of the infarct-related artery (i.e., STEMI).

There were 3534 other STEMIs in this study, not including the 314 with ST depression only (posterior STEMI). Add these 314 to the 3534 and you have 314/3848 (8.1%) of STEMI have pure isolated posterior STEMI. This conforms with the previous smaller studies. Moreover, the cath was done a median of 29.4 hours after presentation, so this does not account for those arteries that spontaneously reperfused (about 25% of STEMI will reperfuse with antiplatelet and antithrombotic therapy alone within one day -- old data). Thus, there were probably even more occluded arteries.

Only 14/314 (4.5%) were interpreted by the investigator as STEMI. None of the patients with an occluded artery had an ECG to PCI time <6 hours.

This is not a "rare" event.

Subacute STEMI Masked by a Wide Complex

See this post for a wide complex that reveals the MI.

Case:
This 46 yo male with no h/o MI or coronary disease presented with 2 days of palpitations, nausea and dizziness and intermittent chest pain that started while walking. The chest pain was never prolonged and constant. Here is his initial ECG (816 AM):

There is occasional sinus rhythm (beats 2, 7, and 13) with narrow complex and the remainder have an uncertain origin (left bundle escape rhythm?) with RBBB morphology. Leads V1-V3 have no complex that is narrow. Narrow complexes can be seen in other leads and V4 is most remarkable, with minimal if any R-wave, then ST elevation and biphasic T (up then down). This is highly suspicious for MI.

V1-V3 have RBBB morphology, but the initial r of the rSR' is replaced by a Q-wave. V3 has an RBBB pattern with ST elevation. There is 1 mm of ST elevation in V1-V3 in the presence of RBBB; this is abnormal, but when there is a Q-wave, it can be due to old MI with persistent ST elevation. ST segments in RBBB in V2 and V3 are usually negative, opposite the tall R' wave. Any ST elevation is abnormal.

This was unrecognized, and at 941 AM another ECG was recorded:

In this recording, the 4th and 10th complexes are narrow, and the 5th and 11th appear to be fusion beats. ST elevation remains in V3 (abnormal, diagnostic of old or new MI). V4 still has biphasic T-waves.

At this point, the troponin returned at 81 ng/ml and the cath lab was activated. A 70% ulcerated lesion with thrombus was found in the proximal LAD. Thrombus was suctioned and stent placed. Here is the post cath ECG:

Finally we have a QRS that is of normal duration, and it has the classic biphasic T-waves of Wellens' syndrome, but is NOT Wellens'. Why? Because Wellens' syndrome has preservation of R-waves. Wellens' is a sentinel event, warning of massive MI. In this case, the massive MI has completed and there are QS-waves.

Here are many cases discussing Wellens' syndrome, and here is one in particular that shows the classic progression over time.

The troponin peaked at 175, there was a large anterior, septal and apical WMA with EF of 40%.

Here is a slightly later recording:

During this recording, the patient was again going in and out of RBBB (RBBB in complexes 1, 3, 9, and 10; 8 and 11 are fusion beats), and you can see how the T inversion in V4-V6 (where there are no normal complexes) is completely hidden by the RBBB morphology. RBBB has rendered the T waves upright.

This was recorded 3 days later:

The escape rhythm with RBBB morphology remains, and all T-wave changes are obscured.  Thanks to VinceD for recognizing the retrograde (inverted) p-waves buried in each RBBB complex.

Summary:

1) For help in diagnosis, look for the complexes that have a normal QRS
2) In RBBB, any ST elevation in V1-V3 is abnormal

3) Q-waves in RBBB, with ST elevation, may be subacute MI or old MI with persistent ST elevation.

Tachycardia must make you doubt an ACS or STEMI diagnosis; put it all in clinical context

This 54 year old patient with a history of kidney transplant with poor transplant function had been vomiting all day when at 10 PM he developed severe substernal crushing chest pain. He presented to the Emergency Department with a blood pressure of 111/66 and a pulse of 117. He had this ECG recorded. He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG:

There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. There is reciprocal ST depression in I and aVL. At first glance, it seems the patient is having a STEMI.

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But, remember, we do not evaluate and treat ECGs, we evaluate and treat patients. Even if this ECG is the first thing one sees (as it was for me), one should stop and think: "This is an unusual STEMI." Why?

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ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock. Are the lungs clear? Is the patient cool and pale? Then ACS (STEMI) might be primary; this might be cardiogenic shock.

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More often, tachycardia with ST segment abnormalities (elevation or depression) is due to an underlying illness (PE, sepsis, hemorrhage, dehydration, hypoxia, respiratory failure, etc.). One must clearly rule out these processes before jumping on the ACS diagnosis.

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Furthermore, notice the well-formed Q-waves in inferior leads. These must raise suspicion of old MI with persistent ST elevation.

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One very useful adjunct is ultrasound: Echo of his heart can distinguish aneurysm from acute MI by presence of diastolic dyskinesis, but it cannot distinguish demand ischemia from ACS.  In this case, bedside echo did not reveal a no wall motion abnormality, but there was hyperdynamic function, which is not consistent with cardiogenic shock but rather with sepsis or volume deficit.

Large volume fluid resuscitation was undertaken. The K returned at 6.9 mEq/L. The HCO3 was 8. Cr was 13.4. Even after 3 liters of fluid, his CVP was very low.

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Troponins peaked at 0.275 ng/ml. An angiogram showed no acute coronary lesions. The patient was suffering from severe dehydration, possibly with sepsis.

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After stabilization, old EKGs and an old echocardiogram were found, with the ECGs demonstrating old inferior MI with persistent ST elevation (LV aneurysm morphology) and the echo showing diastolic dyskinesis.

Pseudoinfarction patterns: there are many and this is one: what is it?

This is courtesy of Mohammed S. Alo, who kindly let me reproduce a case from his blog (Mohammed Alo's blog).

This is a 40 year old male with chest pain. The cardiologist was called for management of a STEMI:


It is sinus rhythm, and there is slightly wide and abnormal appearing QRS, with an rSR' (though I don't think the duration is long enough to be RBBB, but that is a bit hard to read). There is significant ST elevation in V2 and some in V3.  There is "saddleback" ST elevation.  However, it just does not have the appearance of anterior STEMI.

First, when assessing any ST-T abnormalities, one must determine if they are "primary" (due to pathology such as ischemia or hypokalemia, etc.) or "secondary" to an abnormal QRS. And here the QRS is abnormal. Then, think if it conforms to any known pathologic morphology. If you do, and you are aware of the 3 forms of Brugada syndrome, you will see that this is very similar to Type II Brugada.


Here is another case with "saddleback" ST elevation.

Here are the 3 types:

Type I: ("Coved type") V1 has an incomplete RBBB, a wide R' wave, a downsloping ST segment, and in inverted T-wave, like this:

Types II and III) These have a saddle back ST-T wave, as in the case presented. The ST segment is at least 1 mm in Type II and less than 1 mm in Type III

There are also variants of early repolarization that can mimic Brugada. Here is one that mimics type III Brugada (again, sorry it cannot be enlarged):

Case conclusion: the man did indeed have Type II Brugada ECG, not Anterior MI.

Brugada pattern ECG does not necessarily mean the patient has Brugada syndrome.  Here are the 2002 consensus diagnostic criteria for Brugada syndrome.

Type I Brugada

Appearance of type 1 Brugada pattern in more than one right precordial lead (V1-V3) in the presence or absence of a sodium channel blocker, and at least one of the following:
1) Documented ventricular fibrillation

2) self-terminating polymorphic ventricular tachycardia (VT)

3) Family history of sudden cardiac death at <45 years

4) Type 1 ST segment elevation in family members
5) Electrophysiologic inducibility of VT
6) Unexplained syncope suggestive of a tachyarrhythmia
7) Nocturnal agonal respiration

Type 2 and type 3 Brugada syndrome — a type 2 or type 3 Brugada ECG who meet both of the following criteria [7]:

1) Appearance of type 2 or type 3 ST segment elevation (saddle-back type) in more than one right precordial lead under baseline conditions, with conversion to type 1 following challenge with a sodium channel blocker.

2) One of (a-g) above.

•Appearance of type 1 ST segment elevation (coved type) (figure 2) in more than one right precordial lead (V1 - V3) in the presence or absence of a sodium channel blocker, plus at least one of the following:

a) Documented ventricular fibrillation
b) Self-terminating polymorphic ventricular tachycardia (VT)
c) Family history of sudden cardiac death at <45 years
d) Type 1 ST segment elevation in family members
e) Electrophysiologic inducibility of VT
f) Unexplained syncope suggestive of a tachyarrhythmia
g) Nocturnal agonal respiration

Subtle ST elevation in acute LAD occlusion; persistent ST elevation due to poor microvascular perfusion

Inferior STEMI: can we predict the infarct related artery?

Inferior STEMI may be due to RCA or circumflex occlusion (and occasionally due to a "Type III" or "wraparound" LAD, with concomitant anterior MI). If inferior STEMI is due to RCA occlusion, then the right ventricle may be involved, and a right sided ECG is indicated. If due to circumflex, then one need not worry about RV MI. In addition, the interventionalists like to know which artery is involved before the angiogram, if possible.

Here is the ECG of a previously healthy 35 year old male with one hour of chest pain:

There is obviously an inferior STEMI.

Notice:

1. There is no reciprocal ST depression in lead I

2. There is ST elevation in leads V5 and V6.

3. ST elevation in lead II is at least as high as that in lead III

These are 3 criteria which are highly correlated with circumflex occlusion.

Kontos MC et al. Am J Cardiol 1997;79:182

Chia BL et al. Am J Cardiol 2000;86:341

Bairey CN et al. Am J Cardiol 1987;60:456

DeVerna et al. (including Kurz MC and Smith SW) has more recently developed a decision rule (see diagram), presented at ACEP Research Forum in 2008 [DeVerna CJ et al. Ann Emerg Med2008;52(4 Suppl):S117.]. We are in the process of validating this tool. A score greater than or equal to 5 diagnosed circumflex occlusion with very high specificity.

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Cardiac Arrest, acute ST elevation and depression superimposed on LVH, but NOT due to ACS

This young male had ventricular fibrillation during a triathlon. He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. On his bib it stated that he had a congenital heart disorder. He arrived in the emergency department hemodynamically stable. His initial ECG is shown here.

There is profound LVH with anterolateral ST elevation and reciprocal ST depression in II, III, aVF, and ST depression in V5 and V6 that could all be secondary to LVH or could represent ischemia superimposed on the  repolarization abnormalities of LVH: note that wherever there is ST depression, it is associated with a very high voltage R-wave.  The ST elevation in V1-V3 is typical of LVH (high voltage S-waves), but the ST elevation in aVL is concordant to (in the same direction as) the high voltage and thus very suggestive of injury pattern.

ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS.

 A bedside echo performed by the emergency physician showed no wall motion abnormality and confirmed LVH. A repeat ECG after a few minutes of cool down is shown.

Now there is much less ST segment deviation, less elevation and less depression.

The troponin returned positive, and the maximum troponin was 3.8 ng/ml. The next day, and angiogram showed normal coronary arteries. An echocardiogram confirmed aortic stenosis with a large pressure gradient. The stress of the triathlon cause demand ischemia and ventricular fibrillation.  He awoke and did  well.

Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI.

Wide Complex Tachycardia converted, subsequent 12-lead with ST elevation due to WPW

This 58 yo male with a PMHx only significant for Sleep Apnea felt dizzy, lightheaded and nauseated after exerting himself, with no CP or SOB. He subsequently had a syncopal event and was down for 1-2 minutes. His wife called 911. EMS found him with an irregular heart rate at 200-250 beats per minute. He was electrically cardioverted to sinus rhythm. Upon arrival to the ED, he had the following 12-lead ECG:

There is striking ST segment elevation in V1 and V2, with ST depression in V3-V6 as well as I, II, and aVF. There is also a wide QRS. One might think this represents acute STEMI, or Bundle branch block with discordant ST segments and suspicously concordant T-waves.

However, closer inspection reveals a very short PR interval and that the wide QRS is due to a slurred upstroke (delta wave).

This is WPW, which is well known to produce pseudoinfarction patterns.

The patient had a positive troponin, underwent cath which showed completely clean coronaries, and then underwent EP testing which revealed that, in atrial fibrillation, he has an R-R interval as short as 220 ms, which is dangerously short. Ablation was planned for a later date.